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Journal of Dental Research, Vol. 85, No. 5, 473-478 (2006)
DOI: 10.1177/154405910608500515

Clinical

Peri-implant Inflammation Defined by the Implant-Abutment Interface

N. Broggini1,5, L.M. McManus1,2, J.S. Hermann1,3, R. Medina4, R.K. Schenk5, D. Buser5 and D.L. Cochran1,*

1 Departments of Periodontics and
2 Pathology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA;
3 Division of Periodontics and Implant Dentistry, Stuttgart Continuing Education Center, German Dental Association, Stuttgart, Germany;
4 Department of Dental Research, Universidad Autonoma de Coahuila Facultad de Odontologia, Torreon, Mexico; and
5 Department of Oral Surgery and Stomatology, School of Dental Medicine, University of Bern, Switzerland

Correspondence: * corresponding author, cochran{at}uthscsa.edu

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 ± 691 vs. 2398 ± 1077 neutrophils/mm2). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.

Key Words: bone loss • implant-abutment interface • inflammation • microgap • neutrophil


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